In vivo and in vitro effects of somatostatin and insulin on glucagon release in a human glucagonoma.

Détails

ID Serval
serval:BIB_03EC0141AEE8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
In vivo and in vitro effects of somatostatin and insulin on glucagon release in a human glucagonoma.
Périodique
Clinical endocrinology
Auteur(s)
Waeber G., Gomez F., Chaubert P., Temler E., Chapuis G., Boulat O., Nicod P., Haefliger J.A.
ISSN
0300-0664
Statut éditorial
Publié
Date de publication
1997
Peer-reviewed
Oui
Volume
46
Numéro
5
Pages
637-42
Langue
anglais
Notes
Publication types: Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't - Publication Status: ppublish
Résumé
Inhibition of pancreatic glucagon secretion has been reported to be mediated by glucose, insulin and somatostatin. As no human pancreatic alpha-cell lines are available to study in vitro the relative importance of insulin and glucose in the control of pancreatic glucagon release, we investigated a patient presenting with a malignant glucagonoma who underwent surgical resection of the tumour. Functional somatostatin receptors were present as octreotide administration decreased basal glucagon and insulin secretion by 52 and 74%, respectively. The removed tumour was immunohistochemically positive for glucagon, chromogranin A and pancreatic polypeptide but negative for insulin, gastrin and somatostatin. The glucagonoma cells were also isolated and cultured in vitro. Incubation experiments revealed that change from high (10 mM) to low (1 mM) glucose concentration was unable to stimulate glucagon secretion. A dose-dependent inhibition of glucagon release by insulin was however, observed at low glucose concentration. These findings demonstrate that insulin could inhibit glucagon secretion in vitro in the absence of elevated glucose concentrations. These data suggest, as observed in vivo and in vitro in several animal studies, that glucopenia-induced glucagon secretion in humans is not mediated by a direct effect of low glucose on alpha-cells but possibly by a reduction of insulin-mediated alpha-cell suppression and/or an indirect neuronal stimulation of glucagon release.
Mots-clé
Chromogranin A, Chromogranins, Depression, Chemical, Glucagon, Glucagonoma, Glucose, Hormones, Humans, Immunohistochemistry, Insulin, Male, Middle Aged, Octreotide, Pancreatic Neoplasms, Pancreatic Polypeptide, Tumor Cells, Cultured
Pubmed
Web of science
Création de la notice
17/11/2008 9:57
Dernière modification de la notice
20/08/2019 13:25
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